Anaemia in GIT disorders can be simply considered against some of the commoner problems arising through the GIT:

Oesophageal—bleeding from peptic oesophagitis, association of oesophageal web and chronic Fe deficiency.

Gastric—pernicious anaemia and B12 deficiency, late effects of partial or total gastrectomy producing B12 and/or Fe deficiency. Microangiopathic haemolytic anaemia from metastatic adenocarcinoma.

Small bowel—malabsorption states e.g. Fe and/or folate deficiency 2° to coeliac disease, malabsorption from other problems including inflammatory bowel disease; hyposplenism secondary to coeliac with or without 4 platelets.

Large bowel—blood loss anaemia from inflammatory bowel disorders. Note, these may also be associated with ACD. Rare occurrence of autoimmune haemolysis associated with ulcerative colitis.

Pancreas—anaemia of chronic disease associated with carcinoma or chronic pancreatitis, DIC associated with acute pancreatitis.

Drug related anaemia arises through

• Upper GIT irritation causing blood loss—aspirin, NSAIDs, corticos-teroids.

• Bleeding due to specific drugs e.g. warfarin and heparin.

• Drug-induced haemolysis e.g. oxidative (Heinz body) haemolysis due to sulphasalazine or dapsone.

• Production impairment e.g. aplasia secondary to mesalazine.

Anaemia is common in chronic liver disorders. There are several possible causes including:

• Anaemia of chronic disease—part of marrow response to chronic inflammatory processes.

54 • Macrocytosis ± anaemia: specific effects on membrane lipids cause 4 MCV.

• Alcohol—direct suppressive effect on erythropoiesis with 4 MCV.

• Folate deficiency: seen in alcoholic liver disease—^nutritional deficiency and/or direct effect of alcohol on folate metabolism.

• Blood loss from oesophageal varices—»acute or chronic anaemia.

• Hypersplenism—portal hypertension can produce marked splenic enlargement leading to hypersplenism.

• Haemolytic anaemias e.g.

- Autoimmune haemolytic anaemia in association with chronic active hepatitis.

- Zieve's syndrome (hypertriglyceridaemia + self-limiting haemolysis due to acute alcohol excess).

- Viral hepatitis may provoke oxidative haemolysis in those with G6PD deficiency.

- Acute liver failure—DIC and MAHA may occur.

- Acanthocytosis: acute haemolytic anaemia with acanthocytosis (spur cell anaemia). Rare. Usually late stage liver disease, with poor prognosis.

Microcytic anaemia is common and the commonest cause is chronic iron deficiency.

Iron physiology and metabolism jg Normal (Western) diet provides @15mg of iron/d, of which 5-10% is absorbed in duodenum and upper jejunum. Ferrous (Fe2+) iron is better absorbed than ferric (Fe3+) iron. Total body iron store @ 4g. Around 1mg of iron/d lost in urine, faeces, sweat and cells shed from the skin and GIT. Iron deficiency is commoner in 3 of reproductive age since menstrual losses account for ~20mg Fe/month and in pregnancy an additional 500-1000mg Fe may be lost (transferred from mother—► fetus).

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